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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2004-3-30
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pubmed:abstractText |
The nonapoptotic functions of Fas ligation are incompletely characterized. In contrast to expectations, we show here that Fas-deficient mice developed less-severe collagen-induced arthritis than did control mice. Despite having milder arthritis, Fas-deficient mice had more of the critical pro-inflammatory mediator interleukin-1 beta (IL-1 beta) in their joints, suggesting inefficient activation through IL-1 receptor 1 (IL-1R1) when Fas signaling is deficient. In primary human macrophages and macrophages from Fas- or Fas ligand (FasL)-deficient mice, interruption of Fas-FasL signaling suppressed nuclear factor-kappa B activation and cytokine expression induced by IL-1 beta and lipopolysaccharide. This cross-talk was mediated by the Fas-associated death domain through interaction with myeloid differentiation factor 88. These observations document a unique mechanism whereby Fas-FasL interactions enhance activation through the IL-1R1 or Toll-like receptor 4 pathway, which may contribute to the pathogenesis of chronic arthritis.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Signal Transducing,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/FADD protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/FASLG protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Fadd protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fas-Associated Death Domain Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fasl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/TLR4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1529-2908
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
380-7
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:15004557-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:15004557-Animals,
pubmed-meshheading:15004557-Antigens, CD95,
pubmed-meshheading:15004557-Arthritis, Experimental,
pubmed-meshheading:15004557-Carrier Proteins,
pubmed-meshheading:15004557-Fas Ligand Protein,
pubmed-meshheading:15004557-Fas-Associated Death Domain Protein,
pubmed-meshheading:15004557-Humans,
pubmed-meshheading:15004557-Inflammation,
pubmed-meshheading:15004557-Interleukin-6,
pubmed-meshheading:15004557-Lipopolysaccharides,
pubmed-meshheading:15004557-Macrophages,
pubmed-meshheading:15004557-Membrane Glycoproteins,
pubmed-meshheading:15004557-Mice,
pubmed-meshheading:15004557-Receptors, Cell Surface,
pubmed-meshheading:15004557-Receptors, Interleukin-1,
pubmed-meshheading:15004557-Toll-Like Receptor 4,
pubmed-meshheading:15004557-Toll-Like Receptors
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pubmed:year |
2004
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pubmed:articleTitle |
Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation.
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pubmed:affiliation |
Northwestern University Feinberg School of Medicine and Veteran's Administration Medical Center, Chicago, Lakeside Division, Department of Medicine, Division of Rheumatology, 300 E. Superior Avenue, Tarry 3-713, Chicago, Illinois 60611, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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